Central alpha-2 adrenergic mechanisms in the renal nerve mediated natriuresis and diuresis produced by acute volume expansion

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Abstract

To determine whether central alpha-2 adrenergic mechanisms are involved in the renal nerve mediated natriuresis and diuresis produced by acute volume expansion, urine flow and sodium excretion from innervated and denervated kidneys were measured before and after acute volume expansion (1 ml/min for 20 min) in the presence or absence of intracerebroventricular yohimbine (8 μg/kg/min), an alpha-2-antagonist, in Inactin-anesthetized Sprague-Dawley rats. The innervated to denervated (I/D) ratio for urine flow and sodium excretion indicated that acute volume expansion caused a greater natriuresis and diuresis from the intact kidney compared to the denervated kidney. However, these I/D ratios during acute volume expansion were significantly reduced in the presence of yohimbine i.c.v. Furthermore, central administration of clonidine, an alpha-2 agonist, produces a renal nerve mediated natriuresis. These data suggest that central alpha-2 adrenergic mechanisms may be involved in producing the renal sympatho-inhibition, which subsequently produces natriuresis and diuresis, in response to acute volume expansion.

Original languageEnglish (US)
Pages (from-to)47-59
Number of pages13
JournalJournal of the Autonomic Nervous System
Volume37
Issue number1
DOIs
StatePublished - Jan 1992

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Natriuresis
Diuresis
Adrenergic Agents
Kidney
Yohimbine
Sodium
Urine
Clonidine
Sprague Dawley Rats

Keywords

  • Central alpha-2 receptor
  • Natriuresis
  • Renal nerve
  • Volume expansion

ASJC Scopus subject areas

  • Neuroscience(all)
  • Physiology
  • Clinical Neurology

Cite this

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abstract = "To determine whether central alpha-2 adrenergic mechanisms are involved in the renal nerve mediated natriuresis and diuresis produced by acute volume expansion, urine flow and sodium excretion from innervated and denervated kidneys were measured before and after acute volume expansion (1 ml/min for 20 min) in the presence or absence of intracerebroventricular yohimbine (8 μg/kg/min), an alpha-2-antagonist, in Inactin-anesthetized Sprague-Dawley rats. The innervated to denervated (I/D) ratio for urine flow and sodium excretion indicated that acute volume expansion caused a greater natriuresis and diuresis from the intact kidney compared to the denervated kidney. However, these I/D ratios during acute volume expansion were significantly reduced in the presence of yohimbine i.c.v. Furthermore, central administration of clonidine, an alpha-2 agonist, produces a renal nerve mediated natriuresis. These data suggest that central alpha-2 adrenergic mechanisms may be involved in producing the renal sympatho-inhibition, which subsequently produces natriuresis and diuresis, in response to acute volume expansion.",
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AB - To determine whether central alpha-2 adrenergic mechanisms are involved in the renal nerve mediated natriuresis and diuresis produced by acute volume expansion, urine flow and sodium excretion from innervated and denervated kidneys were measured before and after acute volume expansion (1 ml/min for 20 min) in the presence or absence of intracerebroventricular yohimbine (8 μg/kg/min), an alpha-2-antagonist, in Inactin-anesthetized Sprague-Dawley rats. The innervated to denervated (I/D) ratio for urine flow and sodium excretion indicated that acute volume expansion caused a greater natriuresis and diuresis from the intact kidney compared to the denervated kidney. However, these I/D ratios during acute volume expansion were significantly reduced in the presence of yohimbine i.c.v. Furthermore, central administration of clonidine, an alpha-2 agonist, produces a renal nerve mediated natriuresis. These data suggest that central alpha-2 adrenergic mechanisms may be involved in producing the renal sympatho-inhibition, which subsequently produces natriuresis and diuresis, in response to acute volume expansion.

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